Monthly Archives: November 2010

Midst all the hype about driving all older women to annual xray screening mammography for decades- in the end, for no proven net benefit except $billions in profits to the Disease Industry- one of the most pernicious tools used in the mammographysaveslives campaign has been scaremongering.

Winnifred Cutler and a team from the American Colllege of Obstetricians and gynecologists and Switzerland have done women an enormous service in analyzing 18 recent studies covering over 1.8million women from North America and Europe – “a tough search for unbiased data”.

They find that contrary to marketing mythology that women have a 32% lifetime risk of breast cancer (based on ‘massaging’ of American data claiming that breast cancer is the 2nd commonest cause of women deaths), it comes in 5th at 30 deaths per 100 000 women, way behind heart, stroke, lung disease and lung cancer totalling 460 per 100 000.

In fact, even although these modern studies analysed include breast cancers detected by xray screening mammography, the incidence of breast cancer is only about 0.13% per year in the plausible UK Mam Screen of 39000 women; 0.2%pa in the US 283000 women trial; 0.3%pa in the Finnish Registry; and 0.3%pa in the Womens’ Health Initiative.

And in fact even in the bad UK Million Women Study (it enrolled only volunteers), the incidence was only <0.25%pa.

Since average postmenopausal women have a life expectancy to 85yrs average, from average menopause at 52yrs, the above studies give them a lifetime postmenopausal breast cancer expectancy of (33 x 0.3=) 10% ie 1 in 10.

But in fact, if the risk is 10% in their last 35yrs of life. and far lower before that, – and in poor countries average womens’ life expectancy is still barely to average menopause age- their lifetime risk is more like (10% x 33/85=) 4%.

But that 1:10 number in published studies included those detected by xray screening mammography, the majority of cancers which it is now argued may be overdiagnosed, would never have presented clinically during their lifetime.

Thus the true incidence of breast cancer post menopause is probably below 1 in 1000 per year, over a lifetime far below 1 in 10, not 1 in 8 or even 1 in 3 as diseasemongering would have women believe.

CONCLUSION: the real risk of breast cancer (in those without a serious family genetic risk) is far lower than claimed by the Breast Cancer Industry. Such deliberate scaremongering is a major weapon in the war for profit.

Question: Some say that ‘progesterone / progestins worsen bone loss’. everything I’ve read about progesterone says the opposite. In fact Dr John Lee wrote a book about it.

Answer: Most published stuff is rehash, opinion- not evidence.

Dont forget that Drs John Lee & Kathy Dalton never did or published a trial, merely their opinions. They wrote books and articles based purely on subjective experience- and didnt have Medline to give them evidence.. They probably benefitted millions of women by advocating at least some safe progesterone cream replacement that was undoubtedly a lot better than nothing. But all one can do from observations is formulate a theory, a hypothesis. Massive evidence is accumulating that all men and women with low progesterone should supplement with it to around a level of 1 -2 nmol/L for immune and neuroprotective -benefits; – but to no clear benefit against fractures when used alone.

No significant reported trials of progesterone or it’s synthetics that one can find, including from the top Osteoporosis reseach units in the world, show benefit of any progestin on its own on fracture risk – if anything the contrary– in postmenopausal women

[It is unclear from published trials whether adding strontium, biphosphonates, SERM, calcitonin, parathyroid hormone , or human growth hormone in HGH-deficient elderly patients, further reduces fracture rates when added to appropriate essential supplements already listed above – this seems unlikely. and no Drug manufacturer is going to fund such a trial, which will likely only confirm the fruitlessness and risks of their exensive patent drugs] . .

Estrogen at best stops bone loss- and in the WHI, reduced fractures by just below a third . When combined with progestin, th anti-fracture benefit was slightly reduced.

What matters is that only vigorous vit D & appropriate testosterone actually restore lost bone and muscle mass / strength.

Bone density improvement on progesteronealone has been claimed, but there are no definitive studies in humans or animals to show this.

We do know that the synthetic progestins if anything reduce bone density EXCEPT perhaps the androgenic progestins -which progesterone is not. !

In the two arms of the giant Womens’ Health Initiative, in well-matched women, compared to placebo, premarin alone reduced all fractures by 29% (and hip fractures by 35%) whereas premarin + progestin reduced all by only 23% (and hip fractures by 33%) .

In the PEPI and the Lydeking-Olsen trials, progestins at least stopped fall in bone density- but only in the WHI did estrogen reduce fractures- and progestin did not help further.

So where are the trials showing that progesterone actually does reduce fractures? It will be great to see them.

However, in a landmark review that matches her study-of-the decade on the Perimenopause in 1998 (showing that that phase is in fact a time of estrogen excess) – Jerilyn Prior last month published with Seifert-Klauss another study-of-the-decade showing that progesterone itself is in fact a vital co-hormone in enhancing the bone-strengthening effect of estrogen provided they are given together continuously.

How much better against fractures is estrogen+progesterone than estrogen alone? There is still no objective data- but such a trial by Seifert-Klauss ea is in progress.

And given their increased cancer and cardiovascular risks, synthetic progestins ‘ theoretical bone benefits cannot be extrapolated to human progesterone.

But there is so much other evidence about the independent multisystem benefits of progesterone without estrogen – especially for its immune, anti-cancer and neuroprotective benefits- to make it obligatory for progesterone always to be prescribed with estrogen, irrespective of hysterectomy status.

Thus John Lee was wrong on progesterone alone against fractures, but correct for the combination of progesterone with estrogen giving better antifracture protection than estrogen alone. .

Steroid physiology course 101 teaches that our bodies convert vitamin C to cholesterol and then PREGNENOLONE – the progenitor of the human adrenal and gonadal steroid hormones. that are formed also in our liver, skin and brain. In turn this grandparent steroid produces PROGESTERONE (- one of the three prime sex hormones- and thence also some the anti-inflammatory (cortisones) sex hormones and the salt-controlling steroid mineralocorticoids: and

DHEA – dehydroepiandrosterone, prasterone – an important sex steroid in its own right, and one of the parents of the main androgen-TESTOSTERONE – and the ESTROGENS.

The above steroid hormones are distinct from the other human steroid hormones, the calciferols (vitamin D) which we make in the skin; and the heart-formed glycosides, which regulate and strengthen the failing heart and may suppress some cancers.

DHEA is by far the most abundant blood steroid hormone, peaking at around 30 years of age, then like most dropping by up to 95% into old age,. DHEA seems to be as a resevoir for our needed androgen and estrogens.

USE AS HRT sex steroid hormone replacement/therapy: There was high hope that DHEA would prove major benefit for many diseases including the major degenerative diseases of aging, systemic lupus, etc; but this has not been confirmed by trials and experience except for osteoporosis in androgen-deficient women. .

The Mayo, Creighton and Cleveland Clinic websites give it a cautious but doubtful nod.

Labrie 2007 showed that DHEA in women preferentially boosts androgen rather than estrogen levels- which explains its energizing and bone-strengthening benefits in women with low androgens ie estrogen dominance.

The last trials of DHEA in osteoporosis (Jankowski 2008 ; von Muhlen 2008) in the elderly showed improvement in women. So this is a potential use in the old.

The two trials published this year of DHEA in systemic lupus (Marder USA and Hartkamp Netherlands) also failed to show significant benefits.

Review by Panjari and Sue Davis 2010 from Monash University found no significant role for oral DHEA in women.

PERSONAL PRACTICAL EXPERIENCE AND CONCLUSION: The only time DHEA is often worth trying, helpful is in the frail elderly – biologically old or past the mid-sixties- with low bloodpressure, low energy, wasting or inflammatory disease, osteoporosis. In such patients one is for obvious reasons very cautious about starting even non-oral testosterone in men, and appropriate ie non-oral testosterone/estradiol/estriol in women. One soon sees whether any dose has any benefit, as compared to balanced titrated testosterone-estradiol-progesterone.

Dr Lee Vliet (endocrinologist in Tucson, Arizona) starts DHEA as low as about 1mg a day ie a quarter or 1/8th of a 25mg tablet to start, repeating the dose every few days and then gradually up to 1/4 to /2 to 1 – 2tabs a day.

The difficulty is the unpredictability of whether metabolism to androgens and estrogens will be balanced, or cause adverse effects through imbalance. Such adversity can be better minimized by using separate non-oral daily testosterone and estrogens, but obviously these are both more emotive and more potent, with sexual overtones that the aged often dont want.

For the frail and old, or those concerned about androgenic/estrogenic adverse effects, an even safer alternative is the human metabolite 7 keto DHEA , which is also like DHEA generally available over the counter. It reputedly cannot be metabolized back to androgen and thus estrogen. Ihler 2003 suggested it useful as a thermogenic agent for Raynaud’s phenomenon ie periodic white cold digits; Some consider it no different from DHEA, some stronger; and worth trying for weight loss.